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Shocking urine
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http://www.kidney-international.org & 2015 International Society of Nephrology Kidney International (2015) 87, 865; doi:10.1038/ki.2014.337
Shocking urine Barry R. Gorlitsky1 and Mark A. Perazella1 1
Nephrology, Yale University, New Haven, Connecticut, USA
Correspondence: Barry Gorlitsky, Nephrology, Yale University, New Haven, Connecticut, USA. E-mail: [email protected]
Figure 1 | Sulfa crystal under 40.
A 53-year-old man with diabetes mellitus who underwent decreased donor kidney transplant 9 months prior presented with cough and dyspnea. Chest computed tomography scan demonstrated multiple bilateral cavitary lesions with surrounding ground glass opacities. Bronchoscopy and bronchoalveolar lavage culture demonstrated Nocardia nova. High-dose oral sulfamethoxazole-trimethoprim (1600–320 mg every 8 h) was initiated. Over the next 3 days the patient developed oliguria and serum creatinine increased from 2.0 mg/dl to a peak of 3.3 mg/dl. Automated urinalysis revealed the following: pH 6.0, small blood, and few amorphous crystals. The nephrologist who performed urine microscopy noted 0–1 amorphous crystals per high-power field with a ‘shock of wheat’ appearance (Figure 1). These were consistent with sulfamethoxazole crystals. The drug was discontinued and meropenem and minocycline were substituted. Hemodialysis was initiated for diuretic unresponsive hypervolemia in the setting of acute kidney injury (AKI). The patient began to recover kidney function after 72 h, and dialysis was discontinued with serum creatinine returning to baseline.
Kidney International (2015) 87, 865
Sulfa-containing medications, especially when used in high doses, may cause crystal-induced nephropathy when risk factors such as volume depletion, underlying kidney disease, and acidic urine are present. AKI generally develops within 7 days of treatment and is often associated with oliguria. Sulfa-containing medications cause AKI through intratubular deposition, and impairment of venous blood flow from interstitial congestion and hemorrhage. Associated interstitial inflammation may also contribute to tubular injury. Treatment consists of intravenous fluid repletion, alkalinization of the urine, and hemodialysis when indicated.1 Sulfa-induced crystal nephropathy is often reversible and should be considered in any patient who develops AKI that is temporally related to exposure to an offending agent. The diagnosis can be made by a simple manual urine microscopy. REFERENCE 1.
Perazella MA. Crystal-induced acute renal failure. Am J Med 1999; 106: 459–465.
865
http://www.kidney-international.org & 2015 International Society of Nephrology Kidney International (2015) 87, 865; doi:10.1038/ki.2014.337
Shocking urine Barry R. Gorlitsky1 and Mark A. Perazella1 1
Nephrology, Yale University, New Haven, Connecticut, USA
Correspondence: Barry Gorlitsky, Nephrology, Yale University, New Haven, Connecticut, USA. E-mail: [email protected]
Figure 1 | Sulfa crystal under 40.
A 53-year-old man with diabetes mellitus who underwent decreased donor kidney transplant 9 months prior presented with cough and dyspnea. Chest computed tomography scan demonstrated multiple bilateral cavitary lesions with surrounding ground glass opacities. Bronchoscopy and bronchoalveolar lavage culture demonstrated Nocardia nova. High-dose oral sulfamethoxazole-trimethoprim (1600–320 mg every 8 h) was initiated. Over the next 3 days the patient developed oliguria and serum creatinine increased from 2.0 mg/dl to a peak of 3.3 mg/dl. Automated urinalysis revealed the following: pH 6.0, small blood, and few amorphous crystals. The nephrologist who performed urine microscopy noted 0–1 amorphous crystals per high-power field with a ‘shock of wheat’ appearance (Figure 1). These were consistent with sulfamethoxazole crystals. The drug was discontinued and meropenem and minocycline were substituted. Hemodialysis was initiated for diuretic unresponsive hypervolemia in the setting of acute kidney injury (AKI). The patient began to recover kidney function after 72 h, and dialysis was discontinued with serum creatinine returning to baseline.
Kidney International (2015) 87, 865
Sulfa-containing medications, especially when used in high doses, may cause crystal-induced nephropathy when risk factors such as volume depletion, underlying kidney disease, and acidic urine are present. AKI generally develops within 7 days of treatment and is often associated with oliguria. Sulfa-containing medications cause AKI through intratubular deposition, and impairment of venous blood flow from interstitial congestion and hemorrhage. Associated interstitial inflammation may also contribute to tubular injury. Treatment consists of intravenous fluid repletion, alkalinization of the urine, and hemodialysis when indicated.1 Sulfa-induced crystal nephropathy is often reversible and should be considered in any patient who develops AKI that is temporally related to exposure to an offending agent. The diagnosis can be made by a simple manual urine microscopy. REFERENCE 1.
Perazella MA. Crystal-induced acute renal failure. Am J Med 1999; 106: 459–465.
865